This invention generally relates to the detection of electrical activity or signals within a patient's heart and particularly for determining the source of signals causing arrhythmia.
Prior methods for treating a patient's arrhythmia include the use of antiarrhythmic drugs such as sodium and calcium channel blockers or drugs which reduce the Beta-adrenergic activity. Other methods include the surgically sectioning the origin of the signals causing the arrhythmia or the conducting pathway for such signals. More frequently, however, to terminate the arrhythmia, the arrhythmogenic site which causes the arrhythmia is destroyed by heat, e.g. applying a laser beam or radio frequency (RF) energy to a desired location on the patient's endocardium.
In the latter instance, the location of the site causing the arrhythmia must be accurately known in order to be able to contact the desired location with a tissue destroying device. A major problem of ablating the arrhythmogenic site, a conductive pathway or a re-entry site is to accurately determine the location and size of the site so that an excessive amount of good tissue is not destroyed adjacent the site to ensure that the arrhythmia does not return. For example, the average arrhythmogenic site consists of about 1.4 cm.sup.2 of endocardial tissue, whereas a re-entrant site might be much larger. RF ablation techniques produce lesions about 0.5 cm.sup.2 in diameter, so a number of lesions may have to be generated in order to completely ablate the area of interest. If the site is not accurately mapped, much of the good tissue surrounding the site will be unnecessarily destroyed.
A variety of methods have been used to detect electrical activity within a patient's heart to facilitate the mapping of such heart signals and to thereby determine the location of the electrical signals causing the arrhythmia.
A number of U.S. Patents describe the use elongated intravascular signal sensing devices which are advanced through the patient's vasculature until the distal portion having sensing electrodes is disposed within one of the heart chambers with the electrodes in contact with the endocardial lining. While this procedure is widely used, it does not always allow the site of arrhythmogenic signals to be accurately determined.
The literature also mentions advancing an intravascular signal sensing device within a patient's coronary artery or coronary sinus or a cardiac vein. However, these methods have been clinical experiment and have not been widely employed.
What has been needed is a method and system for accurately detecting the source of signals which cause the arrhythmia.